Objectives: 

Although the physiological role of 1,2,3,4-tetrahydro-β-carboline (tryptoline) is unclear, recently, the antioxidant properties of tryptoline have been proposed. Lipid peroxidation is the expression of free radical damage in cell membranes. Structural changes in membranes produced during lipid peroxidation disrupt molecular motion in the membrane. Our aim was to assess the ability of tryptoline, to reduce oxidative damage on hepatic membranes.

Materials: 

0,5 mg protein/mL hepatic membranes were incubated with or without tryptoline (0.1, 0.2, 0.4, 0.6 and 1 mM) in a shaking bath at 37°C for 120 min. Lipid and protein oxidation were induced by adding 0,1 mM FeCl3 and 0,1 mM ascorbic acid and incubating at 37°C for 120 min. The reaction was stopped by adding 2 mM EDTA. Membrane fluidity was evaluated using fluorescence spectroscopy. Lipid and protein oxidation were estimated by quantifying malonaldehyde (MDA) plus 4-hydroxyalkenals (4-HDA) concentrations and protein carbonylation, respectively. Statistical comparisons among experimental groups were performed using student's paired t-test with a level of significance of p<0.05.

Results: 

With oxidative stress, membrane fluidity decreased and MDA+4-HDA concentrations and protein carbonylation levels increased. Tryptoline reduced membrane rigidity and the oxidative markers in a concentration dependent manner. The capacities of triptoline to reduce rigidity as well as lipid and protein membrane injuries by 50%, i.e., IC50, were 0.33, 0.63, and 0.52 mM, respectively.

Conclusions: 

Oxidative damage to hepatic membranes was powerfully inhibited for tryptoline. The results presented here suggest that this &#946;-carboline could be another pineal molecule that resists membrane rigidity due to oxidative stress.